While various chemical and physical irritants can cause irritation and even necrosis of the pulp, the most common causes for pulpal inflammation (pulpitis) are bacteria and/or their products entering the pulp through a deep caries lesion or a leaking filling; an inflammatory reaction in the pulp starts long before bacteria invade the pulp tissue. The inflammatory reaction is first initiated by bacterial antigens interacting with the local immune system. As long as the carious lesion has not entered the pulp, the pulpal inflammation is likely to be reversible. However, when the carious lesion does reach the pulp and the hard tissue barrier is breached, bacteria can invade the pulp. Even after this point, the infection may remain relatively superficial and most of the pulp tissue is vital and bacteria free. For this reason, endodontic treatment of pulpitis should be considered to be treatment of an inflammation and prevention of an infection.
In apical periodontitis, bacteria invade further and colonize the entire root canal system. Apical periodontitis is an inflammatory process in the periradicular tissues caused by microorganisms in the necrotic root canal. Accordingly, to promote healing of apical periodontitis, microorganisms within the root canal system must be eliminated.
Apical periodontitis (AP) is caused by microbes, usually bacteria, residing in the necrotic root canal system of the affected tooth. Although healing of the periapical lesion in some rare cases might be prevented by nonmicrobial factors, microbes are always the etiologic factor in apical periodontitis. The microbes present in the necrotic root canal originate from the oral cavity. However, ecology in the root canal environment is the main factor in the selection of the composition of the infective microflora. As a result of the ecologic pressure, primary apical periodontitis (no previous endodontic treatment) is dominated by anaerobic bacteria, with only a few or no facultative or aerobic species per canal. Endodontic treatment, even when unsuccessful, dramatically changes the ecology in the root canal; availability of oxygen and nutrients is different, and in many cases substances with antimicrobial activity are introduced into the root canal, which might further contribute toward a more resistant, facultative microflora. Post-treatment endodontic infections are therefore dominated by ecologically tolerant bacteria and sometimes also by yeasts, which are characterized by higher resistance to treatment procedures and disinfecting agents than the anaerobic microflora in cases of primary apical periodontitis.
On the basis of our knowledge of the etiology of apical periodontitis, there is a strong consensus that elimination of the microbes in the root canal system is the main immediate goal of the treatment to obtain complete healing of the lesion. There is mounting evidence, however, that obtaining sterility of the infected root canal by presently available treatment methods might be more difficult than once thought.
Locally used endodontic disinfectants, either irrigating solutions or interappointment medicaments, are effective against a wide spectrum of microorganisms. They affect a range of vital functions of the microbial cell, resulting rapidly in cell death. Hypochloric acid interferes with oxidative phosphorylation and other membrane-associated functions of the cell as well as DNA synthesis inside the cell. Hypochlorite is effective against bacteria and yeast; even bacterial spores are killed with high concentration (5%) sodium hypochlorite.
Chlorhexidine (CHX) penetrates the outer cell wall layers of the microbes and attacks the inner membrane, cytoplasmic membrane in bacteria and plasma membrane in yeast cells. In high concentrations CHX has the ability to coagulate intracellular constituents of the microbial cells. The antiviral effect of CHX has also been reported.
The exact mechanism of action of iodine compounds is not fully understood, but these compounds also penetrate into the microorganisms and interact with key molecules of the cells (proteins, fatty acids, and nucleotides). Iodine compounds kill their target cells rapidly, and they are active against bacteria (including spores), fungi, and viruses.
Calcium hydroxide has a high pH, which is the main reason for its antibacterial activity. It has been suggested that the hydroxyl ions denature proteins of the cytoplasmic membrane of bacteria, thus killing the cell. It has been shown with Enterococcus hirae that the tolerance to alkaline pH was dependent on a proton antiport system; mutant cells lacking the proton transport system showed highly increased sensitivity to alkali. This was later also confirmed with a strain of E. faecalis. The susceptibility to high pH of enterococci and oral yeasts has been compared and found that yeasts were equally or more resistant to high pH by calcium hydroxide than E. faecalis. It is likely that tolerance of high pH by oral yeasts is also dependent on a proton pump in the plasma membrane of the yeast cells. Nevertheless, in a saturated calcium hydroxide solution (pH≧12.5) in vitro enterococci were killed within 20 minutes and yeasts within 6 hours.
A mixture of tetracycline isomer (doxycycline), acid, and detergent (MTAD) is a new member in the group of antibacterial root canal irrigants. MTAD contains bacteriostatic antibiotic (doxycycline) in high concentration, which might alter its antibacterial effect to bactericidal, although this has not been directly shown. Other components of MTAD include citric acid and TWEEN 80, which together with doxycycline might have a synergistic effect on the bacterial cell wall and the cytoplasmic membrane.
Despite the advances in the development of root canal irrigation compositions noted above, there exists a need for effective and easy to use compositions for root canal irrigation. The present invention fulfills this need and provides further related advantages.